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PubMed1979

Respiratory paralysis to improve oxygenation and mortality in large newborn infants with respiratory distress.

The nonsynchronous respiratory efforts of neonates with surgically correctable disorders may inhibit effective mechanical ventilation. The records of 25 infants treated with metocurine for muscular paralysis to improve mechanical ventilation were reviewed. All patients were greater than 35 (37.6 +/- 2.1) weeks gestation and 2.27 (2.98 +/- .47) kg. All required ventilatory support with an FiO2 of 100%. The mortality rate of this group of infants was 20% as compared with 73% (p < .001) in a similar group of 26 infants managed without paralysis. In 10 of the 25 infants treated with metocurine, pre- and 1 hr postparalysis paO2 values were available. The mean paO2 prior to paralysis was 62 (45--111) mm Hg and the mean post-paralysis paO2 was 144 (75--227) mm Hg, representing at 132% increase in paO2 (p < .001). The mean dosage for metocurine was 3.5 (1.45--6.79) mg/kg/day; however, those requiring paralysis for greater than 7 days showed a dramatically increasing requirement. These preliminary data suggest that respiratory paralysis reduces right-to-left shunting, improves paO2 and decreases mortality in large infants with severe respiratory distress requiring ventilatory support.

Diaphragm↗
PubMed1986

The role of a functionally distinct IgM anti-type III pneumococcal polysaccharide (SIII) in low-dose paralysis to SIII in mice.

Prior treatment (priming) with a weakly immunogenic dose of Type III pneumococcal polysaccharide (SIII) results in the development of an antigen-specific state of unresponsiveness termed low-dose paralysis which is believed to be mediated by suppressor T cells. The present findings show that the passive administration of functionally distinct non-complement-fixing (NCF) IgM anti-SIII antibodies either in monoclonal form or from protein-A absorbed immune serum could significantly suppress the direct plaque-forming cell (PFC) response to an immunogenic dose of SIII administered concurrently. The degree of suppression was comparable with that induced by low-dose paralysis. Low-dose paralysis was consistently induced in athymic (nude) mice 4 days, but not 3 days, after priming with a low dose of SIII, and was associated with the delayed appearance of NCF-IgM anti-SIII in the serum of athymic mice. In contrast, low-dose paralysis was readily induced in normal BALB/c mice 3 days after priming when NCF-IgM anti-SIII antibodies were present. Comparable inhibiton of the direct anti-SIII PFC response was observed when Concanavalin A (Con A) or NCF-IgM anti-SIII serum was administered with SIII antigen. That Con A and NCF-IgM anti-SIII together did not produce additive suppression was attributed to the adsorption of NCF-IgM anti-SIII antibodies to Con A. Complement-dependent single radial haemolysis mediated by CF hybrid IgM/A or CF-IgM anti-SIII serum was blocked by monoclonal NCF-IgM or IgA anti-SIII antibodies and indicated that each of the antibodies was specific for the same SIII-determinant. Evidence is presented to show that low-dose paralysis in the CF-IgM response to SIII is not mediated by suppressor T cells but can be attributed to highly avid NCF-IgM anti-SIII antibodies, formed preferentially to low doses of SIII, being able to reduce the immunogenicity of SIII administered subsequently. We propose that low-dose paralysis to SIII is the result of an immunobiological function of highly avid NCF-IgM anti-SIII antibodies which not only confer resistance against capsulated pneumococci but preferentially bind soluble SIII-antigen to reduce its immunogenicity and thereby protect specific CF-IgM positive B cells from being rendered tolerant by direct contact with higher doses of SIII antigen.

Animals↗
PubMed2002

Respiratory management of diaphragm paralysis.

The diaphragm is the most important muscle of ventilation. Its contraction is key to the development of intrathoracic pressures. Diseases that affect diaphragmatic function result in decreased pressure-generating capacity by the respiratory muscles. If the involvement is severe or if there is underlying respiratory pathology, diaphragmatic paralysis can lead to overt ventilatory failure. Diaphragmatic involvement can occur unilaterally or bilaterally from systemic diseases or from diseases primarily affecting the diaphragm. Whatever the cause, unilateral diaphragmatic paralysis is usually well tolerated if there is no underlying lung or ribcage pathology. However, under conditions of increased loads, unilateral diaphragmatic paralysis can cause dyspnea and hypoxemia and require treatment. Bilateral diaphragmatic paralysis of any etiology is usually symptomatic and may result in ventilatory failure when severe, or when associated with underlying lung pathology. In some patients unilateral or bilateral paralysis can improve spontaneously but usually over prolonged periods of time. In patients with significant symptoms or development of ventilatory failure, symptoms and outcomes are improved by treatment with noninvasive ventilation or, in selected cases of unilateral paralysis, surgical plication of the diaphragm.

Journal Article↗
PubMed1996

Effects of general anesthesia and paralysis on upper airway changes due to head position in humans.

BACKGROUND: In supine patients with their heads in flexion, general anesthesia causes posterior displacement of upper airway structures that is associated with airway obstruction, and extension of the head helps restore patency. However, the independent effects of head position, general anesthesia, and muscle paralysis on upper airway structures are not known. METHODS: Lateral radiographs of the neck were taken in supine patients with the head in flexion and extension, during consciousness, and after induction of general anesthesia and muscle paralysis. The following measurements were made distances from the horizontal plane to the epiglottis, the hyold, and the thyroid cartilage to detect anteroposterior displacements; distances from the transverse plane to the hyold and the thyroid cartilage to detect cephalocaudad displacements; and widths of the oropharynx, the laryngeal vestibule, and the laryngeal sinus. RESULTS: With the head in flexion, anesthesia and paralysis compared with the conscious state caused posterior displacement of the epiglottis, narrowing of the oropharynx, and widening of the laryngeal vestibule. With the head in extension, anesthesia and paralysis compared with the conscious state caused anterior displacements of the epiglottis, the hyold, and the thyroid cartilage, narrowing of the oropharynx, and widening of the laryngeal vestibule and the laryngeal sinus. CONCLUSION: Loss of tonic muscular activity due to anesthesia and paralysis results in anteroposterior displacements of the upper airway structures with flexion and extension of the head that are in the same direction as that of the mandible. Anesthesia and paralysis also widen the dimensions of the larynx. These changes might have implications for instrumentation and protection of the airway during general anesthesia or unconsciousness.

Aged↗
PubMed1982

Short- and long-term effects of paralysis on the motor innervation of two different neonatal mouse muscles.

1. A study was made of short- and long-term effects of paralysis induced by type A botulinum toxin on the development of innervation of mouse muscles. The toxin was injected locally over the tensor fasciae latae (t.f.l.) and gluteus muscles at various times after birth, and the innervation was later examined by intracellular recording and by a histological technique using a reduced silver stain for axons.2. Paralysis induced at 0-4 days of age delayed but did not prevent the eventual elimination of nearly all focal multiple innervation in gluteus muscle fibres, whereas in t.f.l. up to 50% of the fibres remained focally innervated by more than one axon for at least 120 days. There was an associated reduction in the number of muscle fibres in t.f.l. of between 50 and 70%. The biggest reduction in the number of gluteus fibres was under 40%.3. In the t.f.l., paralysis begun at 6-9 days caused the extent of single-site polyneuronal innervation to increase above the level existing at the time of paralysis. Histologically this increase was seen to be due at least in part to the stimulation of nodal sprout growth from a limited number of nodes.4. Motor nerve terminal sprouts were evoked by paralysis at all ages. In mice injected before 4 days of age recovery from the toxin occurred rapidly and without the formation of ectopic synapses by sprouted motor terminals; however, intrafusal motor nerves also sprouted and established a permanent ectopic innervation on surrounding extrafusal muscle fibres.5. The following conclusions are drawn. (a) In some but not all muscles, neonatally induced paralysis can not only temporarily halt elimination of polyneuronal innervation but actually lead to an increase; it is suggested tentatively that this occurs only during the neonatal period because of the availability at that time of endoneurial pathways associated with normal polyneuronal innervation, rather than because of any special neuronal growth potential then. (b) Permanent establishment of focal polyneuronal innervation is due not to stability of presynaptic elements maintained past a critical developmental stage but is associated with substantial losses of muscle fibres, leading to a high ratio of nerve fibres to muscle fibres.

Aging↗
PubMed1983

Congenital horizontal gaze paralysis and ear dysplasia--a syndrome.

A 9-year-old boy with cyanotic congenital heart disease demonstrated congenital horizontal gaze paralysis and dysplasia of the left external and middle ear. Another patient associating congenital horizontal gaze paralysis and left hemifacial atrophy including ear dysplasia had previously been reported. The coincidence of such rare dysgenetic phenomena as congenital horizontal gaze paralysis and ear dysplasia in 2 patients seems to be significant. Since patients with congenital horizontal gaze paralysis often replace lateral gaze by convergence spasms, gaze paralysis sometimes remains undiagnosed. Therefore, when ocular motor disturbance is associated with ear dysplasia, the possibility of congenital horizontal gaze paralysis should be considered.

Abnormalities, Multiple↗
PubMed1996

The effects of neuromuscular paralysis on systemic and splanchnic oxygen utilization in mechanically ventilated patients.

OBJECTIVE: To evaluate the effect of neuromuscular paralysis on systemic and splanchnic oxygen utilization in patients in respiratory failure during controlled mechanical ventilation. SETTING: A university-affiliated teaching hospital. INTERVENTION: Mechanically ventilated patients, who were undergoing hemodynamics monitoring and who had a gastric intramucosal pH (pHi) of less than 7.35, were studied. Prior to paralysis, the patients were sedated with lorazepam and morphine to standard end points, and the cardiac output and oxygenation were optimized. The patients were then paralyzed with doxacurium and the ventilator rate adjusted to keep the PaCO2 at baseline value. The hemodynamic and oxygenation profile and pHi were determined prior to paralysis and repeated 2 to 2.5 h later. RESULTS: Eight patients were studied; their mean age was 63 +/- 8 years and acute physiology and chronic health evaluation II score was 22 +/- 4. The mean fraction of inspired oxygen, positive end-expiratory pressure, and venous admixture ratio prior to the study was 0.7 +/- 0.14, 11.8 +/- 2.4 cm H2O, and 26 +/- 9%, respectively. Prior to paralysis, the mean set assist controlled ventilation rate was 15 +/- 2 breaths/min and the patient rate was 23 +/- 5 breaths/min. With neuromuscular paralysis, the cardiac index fell from 4.6 +/- 2.2 to 4.3 +/- 2.4 L/min/m2 (p=0.1), the oxygen delivery fell from 537 +/- 129 to 471 +/- 95 mL/min/m2 (p=0.03), and the oxygen consumption and extraction ratio fell from 200 +/ 77 to 149 +/- 35 mL/min/m2 (p=0.03) and 36 +/- 5 to 31 +/- 10, respectively (p=0.2). The pHi increased from 7.21 +/- 0.16 to 7.29 +/- 0.1 (p=0.02). CONCLUSION: In critically ill patients in respiratory failure, neuromuscular paralysis decreased whole body oxygen consumption and increased pHi. Presumably, by eliminating the work of breathing, there is a redistribution of blood flow from the respiratory muscles to the splanchnic and other nonvital vascular beds.

APACHE↗
PubMed2004

The role of CD4(+) T cells in biphasic hind limb paralysis induced by the D variant of encephalomyocarditis virus (EMC-D) in DBA/2 mice.

DBA/2 CrSlc mice infected with the D variant of encephalomyocarditis virus (EMC-D) (10 PFU/head) developed biphasic hind limb paralysis due to spinal cord lesion. The early phase lesion was characterized by demyelination with infiltration of macrophages in the funiculus lateraris and the late phase lesion by degeneration of motor neurons with infiltration of CD4(+) T cells in the cornu ventrale. In the present study, treatment with anti-Mac1 monoclonal antibody (MAb) or anti-CD4 MAb prior to virus infection (-3 to -1 days) reduced the early phase lesion and the incidence of the first paralysis. Signals of viral RNAs were observed only in a few oligodendrocytes in the funiculus lateraris. Treatment with anti-CD4 MAb from 31 to 33 days post infection when mice showed recovery from the first paralysis reduced the late phase lesion and prevented the second paralysis. Signals of viral RNAs were still detected in a few degenerated neurons in the cornu ventrale. These results indicate that while macrophages and CD4(+) T cells participate in the early phase lesion and paralysis and only CD4(+) T cells in the late phase lesion and paralysis.

Animals↗
PubMed1994

[Periodic paralysis. Clinical analysis in 20 patients].

Twenty patients with periodic paralysis were evaluated and the aspects studied included epidemiological data, clinical manifestations, ancillary tests, treatment and evolution. Sixteen patients had the hypokalemic form (5 familiar, 5 sporadic, 5 thyrotoxic and 1 secondary). No patient with the normokalemic form was detected. Predominance of men was found (14 patients), especially in the cases with hyperthyroidism (5 patients). No thyrotoxic patient was of oriental origin. Only 4 patients had the hyperkalemic form (3 familiar, 1 sporadic). Attacks of paralysis began during the first decade in the hyperkalemic form and up to the third decade in the hypokalemic. In both forms the attacks occurred preferentially in the morning with rest after exercise being the most important precipitating factor. Seventy five percent of the hyperkalemic patients referred brief attacks (< 12 hours). Longer attacks were referred by 43% of the hypokalemic patients. The majority of the attacks manifested with a generalized weakness mainly in legs, and its frequency was variable. Creatinokinase was evaluated in 10 patients and 8 of them had levels that varied from 1.1 to 5 times normal. Electromyography was done in 6 patients and myotonic phenomenon was the only abnormality detected in 2 patients. Carbonic anhydrase inhibitors, especially acetazolamide, were used for prophylactic treatment in 9 patients with good results in all. Although periodic paralysis may be considered a benign disease we found respiratory distress in 5 patients, permanent myopathy in 1, electrocardiographic abnormalities during crises in 4; death during paralysis occurred in 2. Therefore correct diagnosis and immediate treatment are crucial. This study shows that hyperthyroidism is an important cause of periodic paralysis in our country, even in non oriental patients. Hence endocrine investigation is mandatory since this kind of periodic paralysis will only be abated after return to the euthyroid state.

Acetazolamide↗
PubMedDate not supplied

[Dementia in progressive supranuclear paralysis patients].

INTRODUCTION: Progressive supranuclear paralysis is difficult to detect in its initial stages. Its symptoms are not specific and often the patients are mistaken as Parkinson s disease patients, or even Alzheimer s ones. DEVELOPMENT: Initial features in progressive supranuclear paralysis are typically a gait disorder with frequent falls, behavioral disorder and often dysarthria. The gaze disorder, showing voluntary conjugate gase paralysis is characteristic, but it can appear late in the course of disease. Other motor signs are axial rigidity, bradykinesia, stiffness, and rarely chorea, ataxia, muscle weakness or myoclonus. Pseudobulbar paralysis is the more remarkable clinical finding. These motor symptoms are accompanied by cognitive disturbances, the typical ones of subcortical dementia, with mind slowness, apathy, depression, and, more often that in other primary dementias, psychotic features and relatively early behavioral disorders. A useful feature to distinguish the mental changes of progressive supranuclear paralysis with other primary subcortical dementias is a more remarkable impairment in visuospatial function, because of the need of a good gaze function to accomplish it. Progressive supranuclear paralysis patients work better in verbal tests that in visuospatial test. We try to describe clinical data and evolutive profile of this entity, whose cognitive disturbances as described by Albert in 1974 strongly stabilized the concept of subcortical dementia.

Dementia↗
PubMed1990

[Oculomotor paralysis caused by lesion of the brain stem].

Oculomotor palsies due to lesions of the brain stem may be complete, affecting all types of eye movements in one direction; this reflects a nuclear, internuclear or infractuclear lesion. This may also be disassociated, affecting only one type of eye movements, and this suggests supranuclear lesions. Concerting lateral movements, complete paralysis of abduction, adduction (sparing convergence) or ipsilateral laterality is suggestive of damage to the radicular fibres of the abducencs nucleus (VI), to its internuclear neurons or to the nucleus itself respectively. Isolated paralysis of saccades is in favour of a lesion of the paramedian pontine reticular formation. As regards vertical movements, paralysis of the oculomotor nerve (III), either isolated or associated with complete paralysis of the contralateral rectus superior oculi muscle, suggests a lesion of the radicular fibres of III or of the nucleus itself respectively. Paralysis of downward or both downward and upward saccades indicates the presence of bilateral lesions in the region of the mesencephalic reticular formation. Paralysis of upward saccades alone reflects a unilateral lesion located near the posterior commissure.

Brain Stem↗
PubMed1969

Hyperthyroidism with periodic paralysis.

Hyperthyroidism may be associated with hypokalemic periodic paralysis. Two cases are presented demonstrating intermittent attacks of flaccid paralysis associated with clinical symptoms, signs and laboratory findings of hyperthyroidism. During an attack, one patient had a serum potassium of 2.1 mEq. per litre.Various factors such as trauma, exposure to cold, excessive carbohydrate ingestion and certain medications have been stated to precipitate an episode of paralysis. Attacks may range from mild weakness to generalized flaccid paralysis with loss of deep tendon reflexes. Several reported patients have died owing to cardiac arrest or respiratory paralysis.During attacks, the serum potassium is usually in the range of 2.2 to 3.2 mEq. per litre. It is postulated that a metabolic abnormality affecting the muscle-cell membrane can occur in the hyperthyroid state resulting in a shift of potassium to the intracellular position, thus producing a situation of hyperpolarization of the muscle-cell membrane which in turn alters the muscle contractibility.The importance of recognizing the unusual association of hypokalemic periodic paralysis with hyperthyroidism is stressed because, with successful treatment of the hyperthyroidism, the episodes of paralysis disappear.

Adult↗
PubMed1993

Poliomyelitis and infantile paralysis: changes in host and virus.

Death of motor neurones following invasion of the central nervous system by poliovirus may result in paralysis of specific muscles. Virulence may be tested by injection into monkeys by routes which bypass natural infection. Transmissibility is also very important, but cannot be measured, only inferred. An infection may lead to immunity or paralysis. In epidemics, the highest incidence among children 0-2 years was 2% and among those over 10 years was 25%: these figures fit a model of genetic susceptibility of homozygotes and heterozygotes with phenotypic susceptibility increasing with age. Hypogamma-globulinemics, some neonates and pregnant women are more susceptible than others. Intra-muscular injections may increase the risk of paralysis. Strenuous exercise and IM injections given when poliovirus has already reached the spinal cord can increase the severity of paralysis or convert a non-paralytic attack to paralysis. Although vaccines reduced polio in temperate countries, polio was thought to be no problem in the tropics. Since 1977 polio has been recognised as a massive problem in the third world: because it affects babies and very young children, it is properly infantile paralysis.

Animals↗
PubMed1994

Laryngeal behavior in unilateral superior laryngeal nerve paralysis.

Laryngeal behavior in unilateral superior laryngeal nerve (SLN) paralysis was investigated in animal models and clinical cases. The occurrence of an oblique glottis caused by rotation of the posterior glottis to the paralytic side was the main focus of this study. The animal model study employed live dogs. When the SLN on one side was sectioned, spontaneous phonation did not cause a significantly oblique glottis. When the unaffected SLN was electrically stimulated during spontaneous phonation, an oblique glottis occurred. When the SLN was unilaterally stimulated during spontaneous phonation with both SLNs sectioned, a markedly oblique glottis occurred. In the clinical study, larynges of 17 patients with SLN paralysis were examined during a test task in which a low-pitched phonation was followed by a high-pitched phonation. The purpose of this task was to activate the unaffected cricothyroid muscle during the test phonation. Five patients could not perform the test task. The glottis obviously rotated in 9 patients, whereas no significant rotation of the glottis occurred in 3. One of the latter 3 had an incomplete paralysis, and the other 2 had marked scarring around the laryngeal framework. We conclude that a unilateral SLN paralysis causes a rotation of the posterior glottis to the paralytic side when the unaffected cricothyroid muscle is markedly activated. The test consisting of low-pitched phonation followed by high-pitched phonation is a relatively simple and accurate diagnostic procedure for unilateral SLN paralysis.

Adult↗
PubMed1982

[Histological findings of 15 excised arytenoid cartilages after long-lasting recurrent nerve paralysis (author's transl)].

Histological findings of 15 excised arytenoid cartilages are reported. In all cases there was a long-term recurrent nerve paralysis without additional inflammatory disease. In one of the cases there was fibrosed ankylosis of the cricoarytenoid joint. This is the first report made on the histological findings of the arytenoid cartilage in cases of paralysis. It is confirmed that there is a difference in the joint pathology in cases of immobility due to inflammatory conditions and pure non inflammatory recurrent paralysis. The fixation caused by arthritis of the joint has relatively poor prognosis after surgery while if fixation is due to recurrent nerve paralysis the chances of recovery are good in long-term paralysis.

Ankylosis↗
PubMed1993

Defective aldosterone synthesis associated with hyperkalemic periodic paralysis.

OBJECTIVE: To describe defective aldosterone biosynthesis (corticosterone methyl oxidase type II [CMO-II] deficiency) in a kindred with hyperkalemic periodic paralysis. SETTING: Tertiary care hospital in Madison, Wis. PATIENTS: Individuals studied included a female infant with failure to thrive, hyponatremia, and hyperkalemia; the infant's asymptomatic mother and father; and a maternal aunt and grandmother with hyperkalemic periodic paralysis. INTERVENTIONS: Mineralocorticoid synthetic pathways were analyzed with synthetic adrenocorticotropin stimulation. In one patient with hyperkalemic periodic paralysis, acetazolamide sodium therapy was discontinued and replaced with fludrocortisone acetate therapy. MEASUREMENTS/MAIN RESULTS: Impaired aldosterone synthesis with marked accumulation of mineralocorticoid precursors 18-hydroxycorticosterone and corticosterone indicated severe CMO-II deficiency in the infant. In her relatives and parents, baseline aldosterone levels (74 to 111 pmol/L) were low (reference range, 194 to 830 pmol/L, a nonstricted sodium diet). Serum 18-hydroxycorticosterone levels (442 to 1021 pmol/L) were normal (reference range, 138 to 1270 pmol/L), but ratios of 18-hydroxycorticosterone to aldosterone were abnormally elevated (4.5 to 13.7; reference range, 2.65 +/- 1.86), indicating deficient CMO-II enzyme activity. Acetazolamide therapy was substituted with fludrocortisone therapy in the maternal aunt without return of paralytic symptoms. CONCLUSION: This association of hyperkalemic periodic paralysis with CMO-II deficiency and resolution of paralytic episodes with fludrocortisone therapy suggests a contribution of defective mineralocorticoid-mediated potassium homeostasis to the pathogenesis of hyperkalemic periodic paralysis.

Aldosterone↗
PubMed1992

Facial paralysis due to benign parotid tumors.

On rare occasions, facial paralysis associated with a parotid tumor need not denote malignancy. We present two cases in which, contrary to appropriate conventional wisdom, facial paralysis resulted from benign mixed tumors. Each patient presented over 8 years following primary surgical excision. In neither patient was a mass palpable, and facial paralysis was the sole sign of recurrent disease. Each patient had been followed up for several months with a presumptive diagnosis of Bell's palsy prior to discovery of recurrent tumor by radiologic imaging. In each case, at operation the tumor was found to infiltrate the temporal bone via the stylomastoid foramen. Facial paralysis presumably resulted from extrinsic compression of the facial nerve. These two cases add to the few previous reports of facial paralysis due to benign parotid gland tumors.

Adenoma, Pleomorphic↗
PubMed1975

A simple, single-injection method for inducing long-term paralysis in embryonic chicks, and preliminary observations on growth of the tibia.

A method for inducing paralysis in embryonic chicks is described. This involves single injections of the neuromuscular blocking agents, D-tubocurrarine Chloride or decamethonium iodide, into 10-day embryos. The dose which optimises survival and paralysis is determined along with the effect of the drugs on embryonic growth. Decamethonium iodide at a dose of 1 mg per embryo gave maximum survival and paralysis to 18 days of incubation. Paralysis was assessed by observation of treated embryos in ovo and by examination of embryos removed from their shells between 11 and 18 days of incubation. Embryos were completely paralysed 24 hours post-injection and remained paralysed until 18 days of incubation. Paralysed embryos failed to hatch. Development of the leg musculature was severely retarded in paralysed embryos. This method of inducing paralysis has considerable advantages over previous continuous infusion methods. The growth and collagen content of the tibia in the paralysed embryos was reduced and these results, and other applications of the method, are discussed.

Acetylcholinesterase↗